Estrone increases adenylcyclase activity, and thus maintains the mitoses of the matrix, and the duration of the anagen. It also activates the staminal cells in the early stages of the anagen phase.
Today, it is usual to accept that male androgenetica alopecia is associated with an increase in 5-alpha reductase activity which, genetically, leads to higher levels of diidrotestosteron but this has been studied mainly, if not exclusively, in males. The results obtained have then been referred to women patients, which to my mind is not appropriate and that is why there is talk of Female Androgenetic Alopecia (FAGA). But to give a diagnosis of Androgenetic Alopecia, there are two essential “sine qua non” conditions:
1) the condition must exist in at least one of the biological parents;
2) there must be a significant quantity of androgen hormones.
Essentially, if a woman is bald for genetic reasons then her own mother must be bald, and the baldness must not be due to Areata Alopecia or Telogen Effluvium. In addition, we must remember that androgen levels in a healthy woman are always much lower than in a male. Also, in a male who is being treated with finasterid or dutasterid DHT levels are approximately 10 times higher than those in a healthy woman with alopecia consequently, for female alopecia, “androgenetic” is by no means a good definition. For this reason, in the 1970s and 1980s, to explain the development of Androgenetic Alopecia in otherwise healthy women, reference was made to “an increment in the metabolic use of testosterone (T) and of its being converted cutaneously into diidrotestosterone (DHT)” (Walter P. Ungher,). It was also thought that these women had “a higher degree of follicular sensitivity (?) to the effects of the androgens in the blood” (Thomsen 1979; Mahoudeau; Bardin; Kirschner 1971 – 79). Another hypothesis was that these women had low levels of Sex Hormone Binding Globulin (Anderson 1974).
If we think that baldness process is caused by androgens, then Androgenetic Alopecia would be present only in androgen sensitive areas. In the scalp, these receptors have been found only in frontal areas and in the crown, and not in temple and occipital areas. Indeed, in males, androgenetic alopecia is present only in these areas.
Female Alopecia also appears to be different from Male Alopecia from a clinical point of view:
1) the pattern is centrifugal, and usually of Ludwig type;
2) in women, alopecia usually spreads to areas that are not sensitive to androgens and involves zones that are not affected in Male Androgenetic Alopecia, such as the nape;
3) follicular miniaturization is different. Initially, at least there is no great loss in depth. It is more a question of thickness. The hair shafts become thinner but remain long;
4) Women virtually never become really bald. Usually, it is a question of hypotrichia;
5) 5-alpha reductase inhibitors seem to be practically ineffective in women. At best, they have an almost negligible effect.

From therapeutic point of view high levels of estrogens (during pregnancy, or in contraception) may have a beneficial effect in many cases of female alopecia and estrogens, usually prescribed with antiandrogens that are similar to progesterone, have been used frequently, and have given good results. However, no clinical trials have been undertaken to verify this.
With the exception of a few rare cases of anomalous surrenal or ovarian hormonal production due to enzymatic defects, or to a secreting tumor, in women alopecia is very different to that in males, presumably because of the diverse metabolic and endocrinic traits in the two sexes.
Female Ludwig Alopecia (FAGA) is, in my opinion, nearly always the result of Telogen Effluvium or of low levels in follicular estrone activity! Young women with thin, sparse hair in all parts of the scalp (but especially in crown and frontal areas) whose mothers are often in the same condition, but who have regular menstrual periods, and normal fertility levels, without excessive androgen, in which it is not possible to find clear proof of Telogen Effluvium lead us to consider the possibility of genetic peripheral resistance or of insufficiencies in the production of intrafollicular estrone (deficit of 17 steroid oxydoreductase, aromatase, 3 alpha reductase). These young females are suffering from hypotrichia or alopecia due to local insufficient estrone!

All this is not only academic waffle! It has important therapeutic implications.
5-alpha reductase inhibitors are ineffective in women because they hit the wrong target by trying to inhibit the metabolism of a hormone that is practically absent; whereas, a topical therapy with estrone or 17 alpha estradiol may be effective in many cases.

When a woman is affected only at the top of the head, and has a so-called “tonsure effect”, and especially if she is losing hair at the temples and at the front of her head, then we can say she has a Male Pattern Alopecia, MAGA, and we will have to look for an androgen cause. On its own, a simple micropolycystic ovary (which is not a real illness!) will never cause Male Pattern Alopecia (MAGA), there has to be something more serius, such as a real Policystic Ovary Syndrome, an ovarian or surrenalic androgen secreting tumor, or a surrenalic enzymatic deficiency like a 21 hydroxyilase deficiency.

We can therefore consider that real Androgenetic Alopecia is frequent in men and rare in women and is caused by the conversion of the testosterone into diidrotestosteron. Low Local Estrone Alopecia is caused by local inadequate estrone activity, is frequent in women and is rare (though possible) in men.